F a s c i c u l a r Ta c h y c a rdi a

Rakesh Latchamsetty, MD*, Frank Bogun, MD

KEYWORDS
! Fascicular tachycardia ! Ventricular tachycardia ! Catheter ablation ! Calcium channel blockers

KEY POINTS
! Fascicular ventricular tachycardia (VT) has characteristic ECG findings with a relatively narrow QRS
complex, right bundle branch block (RBBB), and most commonly left axis deviation.
! Fascicular tachycardia is slightly more prevalent in men, usually presents in young adults without
structural heart disease, and has a favorable long-term prognosis.
! The most frequently described tachycardia mechanism is a macroreentrant circuit involving the left
posterior fascicle with an adjacent slowly conducting zone.
! Fascicular tachycardia is usually responsive both acutely and chronically to calcium channel
blockers and resistant to adenosine.
! Catheter ablation offers high success rates for tachycardia elimination with low complication rates.
Ablation can be performed during tachycardia or sinus rhythm.
! The Purkinje fiber system can also be involved in different ventricular arrhythmias in patients with
structural heart disease.

VT emanating from the left fascicular system has
been described as early as 19721 and has
frequently been referred to as verapamil-sensitive
tachycardia or idiopathic left VT. This reentrant in-
trafascicular tachycardia, however, is often but not
universally responsive to verapamil,2 and other
forms of idiopathic left ventricular tachycardia
exist (eg, left ventricular outflow tract tachycardia).
Idiopathic fascicular tachycardia is usually seen
in patients between 15 and 40 years of age without
structural heart disease and has a male predomi-
nance (60%80%).3 The most common presenta-
tion is exercise-induced palpitations but patients
can also present with tachycardia at rest. Occa-
sionally, incessant fascicular tachycardia can
result in development of a tachycardia-induced
cardiomyopathy and patients can present with
symptoms of heart failure.4 Sudden cardiac death
is infrequent in patients with fascicular tachycardia.
Diagnosis of fascicular tachycardia is suggested
by a correlation of symptoms to characteristic
findings on ECG and verified through an
electrophysiology study mapping the tachycardia
to the left fascicular conduction system.
ECG CHARACTERISTICS OF FASCICULAR
ARRHYTHMIAS
There are 3 recognized morphologies of fascicular
VT classified by their regional involvement of the
left fascicular system and characterized by distinct
ECG patterns.5 The most common form involves
the left posterior fascicle and on ECG presents
with a characteristic RBBB with left axis deviation
(Fig. 1). Occasionally, the left anterior fascicle is
involved and the subsequent ECG pattern displays
an RBBB with a right axis pattern (Fig. 2). Rarely,
an upper septal fascicular VT with a narrow QRS
complex and normal or right axis deviation has
also been described. The distribution of these 3
morphologies of fascicular VT are approximately
90%, 10%, and less than 1%, respectively.5,6
Left fascicular arrhythmias should be differenti-
ated from those of papillary muscle origin, which
cardiacEP.theclinics.com

The authors have nothing to disclose.

Department of Internal Medicine, University of Michigan Hospital, 1500 East Medical Center Drive, Ann Arbor,
MI 48109-5853, USA
* Corresponding author. CVC, SPC 5853, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5853.
E-mail address: rakeshl@umich.edu

Card Electrophysiol Clin 6 (2014) 567579

http://dx.doi.org/10.1016/j.ccep.2014.05.006
1877-9182/14/$ see front matter ! 2014 Elsevier Inc. All rights reserved.
568 Latchamsetty & Bogun

Fig. 1. Twelve-lead electrocardiogram of the most common form of fascicular ventricular tachycardia involving
the left posterior fascicle. Note the characteristic right bundle branch block and left axis deviation.

Fig. 2. Twelve-lead electrocardiogram of a fascicular tachycardia involving the left anterior fascicle. Note the
right bundle branch block and rightward axis.

can have a similar axis (Fig. 3). A key distinguish-
ing ECG characteristic between these 2 origins in-
cludes a narrower QRS (127 " 11 vs 150 "
15 milliseconds) in fascicular arrhythmias due to
rapid activation via the specialized conduction
system.7 Another key feature of fascicular arrhyth-
mias is the rsR pattern in V1 indicating that the
initial activation is in the direction of V1 (ie, left to
right) due to the left septal origin. Alternatively,
Fig. 3. Premature ventricular contractions from the left ventricular anterolateral (A) and posteromedial (B) papil-
lary muscles. See text for discussion.
Fascicular Tachycardia 569
arrhythmias originating from the papillary muscles
often have a qR pattern in V1. Fascicular arrhyth-
mias more often have small Q waves in leads I
and aVL, indicating early activation of the septum
from left to right as opposed to a papillary muscle
origin, which is further away from the septum. Ar-
rhythmias originating from the distal Purkinje fiber
system may be mapped to the papillary muscles
close to the Purkinje-myocardial interface.7,8
570 Latchamsetty & Bogun
Both a myocardial origin and an origin from the
Purkinje fiber system have been described for
papillary muscle arrhythmias (Fig. 4).
The use of intracardiac ultrasound has been
particularly helpful in mapping arrhythmias from
the papillary muscles (Fig. 5). Some prior reports
in patients with fascicular tachycardia have
demonstrated the presence of a muscular strand,
or false tendon, in the left ventricle between the
septum and a papillary muscle.9 Excision of this
tendon has been reported to eliminate the tachy-
cardia,10 implicating the false tendon as a potential
critical limb in the reentrant circuit. This finding,
however, has not been universally seen.
In addition to the idiopathic fascicular tachycar-
dias described, several other tachycardias
involving the left fascicular system exist. Bundle
branch reentry tachycardia forms a reentrant cir-
cuit using the His-Purkinje system with involve-
ment of both the left and right bundles and is
usually seen in patients with structural heart dis-
ease. This tachycardia more commonly presents
with antegrade conduction through the right
bundle branch manifesting as a left bundle branch
block morphology on ECG but can also travel in
the reverse direction (Fig. 6) and produce an
RBBB morphology.
Patients postinfarction can also present with VT
with a relatively narrow QRS complex (Fig. 7),
where the tachycardia exit site involves the Pur-
kinje network (Fig. 8). These VTs may be difficult
Fig. 4. Mapping of papillary (PAP) muscle arrhythmias can reveal a site of origin (SOO) either in the distal Purkinje
fibers or in the ventricular myocardium. Note the sharp local Purkinje potentials (arrows) when the SOO is in the
Purkinje fibers.
to distinguish from idiopathic fascicular tachy-
cardia by ECG alone but are also amenable to
catheter ablation.11 Q waves in the inferior leads
are absent in patients with fascicular tachycardia
without structural heart disease; in patients with
prior inferior wall myocardial infarction, however,
Q waves during VT indicate the presence of a prior
myocardial infarction (see Fig. 7). Interfascicular
reentry VT is another distinct ventricular
arrhythmia that can have similar ECG findings
and is usually seen in patients with large anterior
wall myocardial infarctions. In these patients, an
RBBB and delayed conduction in one of the left
fascicles enables a macroreentrant circuit using
both left fascicles. Most often, the anterior fascicle
serves as the antegrade limb and the posterior
fascicle as the retrograde limb (Fig. 9). A hallmark
of interfascicular reentry VT is the similar QRS
complex during sinus rhythm compared with VT
with an RBBB morphology and left fascicular
hemiblock. The His is activated retrograde and
the His to ventricle interval during interfascicular
reentry VT is shorter than during sinus rhythm.5,12
Frequent premature ventricular contractions
(PVCs) can also be localized to the Purkinje system
and be idiopathic or seen in patients with underly-
ing structural heart disease. PVCs from the fascic-
ular system have been reported to trigger
ventricular fibrillation (VF) and can be a cause of
sudden cardiac death.13 PVC ablation in these pa-
tients may eliminate VF triggers.
 Fascicular Tachycardia 571

Fig. 5. Intracardiac echocardiography can offer real-time catheter visualization and facilitate navigation, partic-
ularly in relation to the papillary muscles. The image shows the catheter in contact with the left ventricular
septum (A) and then along a papillary muscle (B). ac, acoustic; MVA, mitral valve annulus; PAP, papillary muscle;
PW, posterior wall. (Adapted from Good E, Desjardins B, Jongnarangsin K, et al. Ventricular arrhythmias origi-
nating from a papillary muscle in patients without prior infarction: a comparison with fascicular arrhythmias.
Heart Rhythm 2008;5:1534; with permission.)

A rare condition has also been described in pa-
tients that can present with frequent multifocal
PVCs emanating from throughout the fascicular
system (Fig. 10). Depending on the PVC burden,
this may result in a PVC-induced cardiomyopathy.
Given the more diffuse involvement of the Purkinje
fiber system, catheter ablation in these patients
can be more challenging. A mutation in the
SCN5A gene has been implicated in a cohort of
such patients and suggests a potential role for
antiarrhythmic medications.14
MANAGEMENT
Medical Treatment
In a patient presenting in VT with ECG and clinical
characteristics of idiopathic fascicular tachy-
cardia, acute management focuses on restoration
of sinus rhythm. Although direct current cardiover-
sion is the preferred method in a hemodynamically
unstable patient, conversion to sinus rhythm in a
stable patient can often be achieved with
intravenous verapamil. Although other idiopathic
left VTs, such as outflow tract tachycardias, are
also frequently sensitive to verapamil, fascicular
tachycardia is differentiated by its resistance to
treatment with adenosine.
It has been suggested that propagation through
a slow conduction zone forms a requisite limb for
reentrant fascicular tachycardia. Conduction
through the distal portion of this zone seems pri-
marily calcium channel dependent and may
explain the sensitivity of fascicular tachycardia to
verapamil.15 Adenosine has been shown to termi-
nate outflow tract tachycardias primarily targeting
cyclic adenosine monophosphate-mediated trig-
gered activity, and the lack of response in fascic-
ular tachycardias lends further support to its
proposed reentrant mechanism.16
Catheter Ablation
Chronic treatment of fascicular tachycardia can
either be pharmacologic or through electrophysi-
ology study and catheter ablation. Despite the
572 Latchamsetty & Bogun
Fig. 6. Twelve-lead electrocardiogram (ECG) of a patient with bundle branch reentry tachycardia. In this example,
the tachycardia propagates antegrade via the left bundle and retrograde via the right bundle, creating a right
bundle branch block morphology on ECG.
effectiveness of intravenous verapamil during
acute management of fascicular tachycardia, the
response to oral verapamil for long-term suppres-
sion is variable.17 In patients in whom symptoms
are refractory to pharmacologic management,
catheter ablation offers an effective and safe treat-
ment option.
Description of recurrent VT sensitive to verap-
amil during electrophysiology study and success-
ful catheter ablation of fascicular tachycardias has
been reported as early as the 1980s.18,19 Pro-
posed mechanisms responsible for the tachy-
cardia include automaticity, triggered activity,
microreentry, and macroreentry.1921 The majority
of evidence supports a macroreentrant circuit
involving most commonly the left posterior fascicle
with an adjacent area of slower conduction, which
may also be part of the Purkinje fiber system.21,22
Different ablation strategies for patients with
suspected fascicular tachycardia have been pro-
posed and have resulted in successful ablation
of fascicular VT. Although this discussion focuses
on patients with fascicular tachycardia involving
the left posterior fascicle, similar strategies are
applied to the left anterior fascicle.
Mapping in patients with documented fascic-
ular VT can be performed during sinus rhythm
or during tachycardia. During sinus rhythm,
Purkinje potentials are recorded along the poste-
rior aspect of the interventricular septum, identi-
fying the course of the posterior fascicle.
Detailed mapping also reveals an adjacent area
with lower-amplitude electrograms, suggesting
the presence of a slow conduction zone involved
in the reentrant circuit (Fig. 11).22 As discussed
later, in patients in whom tachycardia is not
inducible, these serve as potential ablation
targets.
If tachycardia is inducible and tolerated, map-
ping during tachycardia is preferable. Tachycardia
is induced with atrial or ventricular pacing and
sometimes requires administration of isoproter-
enol. The VT reentrant circuit proceeds antegrade
over a zone of slow conduction and retrograde
over the posterior fascicle (Fig. 12).23 The turn-
around point where the antegrade limb connects
to the retrograde limb marks a site where the
earliest Purkinje potentials during VT are recorded.
The exit site is often more distal to this turnaround
point.
Multiple approaches have been described to
target different components of the reentrant cir-
cuit. One approach targets the antegrade limb of
slow conduction during VT, where lower-
amplitude potentials preceding the QRS complex
by approximately 30 to 60 ms22,24 are identified

Fig. 7. Twelve-lead electrocardiogram of a postinfarction ventricular tachycardia with exit site localized to the
left posterior fascicle. Note the relatively narrow QRS complex and Q waves present in the inferior leads.
during late diastole (Fig. 13). Often Purkinje poten-
tials are also present at these sites, indicating
retrograde activation via the posterior fascicle.
The earliest Purkinje potential, which typically pre-
cedes the QRS complex by approximately 15 to
40 ms, can also be targeted.5,22,24 The posterior
fascicle itself can also be targeted and ablation
at any point in its course may eliminate VT. A distal
location is preferable to avoid damage to the prox-
imal conduction system.
Fascicular Tachycardia 573
Mechanical trauma to the fascicles may render
fascicular VTs noninducible. In these patients as
well as in patients without inducible VT at baseline,
ablation is performed during sinus rhythm. Pace
mapping is often used when mapping is per-
formed for reentrant VT in an attempt to identify
the VT exit site. Unfortunately, in fascicular VT,
pace mapping is not as reliable in identifying an
optimal target site for ablation during sinus rhythm
because the critical parts of the reentrant circuit
Fig. 8. Schematic illustration of a
reentrant circuit around an inferosep-
tal scar. Surviving muscle bundles
within the myocardium and in the
Purkinje system are components of
the reentrant circuit with the exit
site at the Purkinje fibers. (From
Bogun F, Good E, Reich S, et al. Role
of purkinje fibers in post-infarction
ventricular tachycardia. J Am Coll Car-
diol 2006;48:2506; with permission.)
574 Latchamsetty & Bogun
Fig. 9. Schematic illustration of an interfascicular
reentrant circuit with antegrade conduction over the
left anterior fascicle and retrograde conduction over
the left posterior fascicle. Note the underlying right
bundle branch block. AVN, atrioventricular node;
HB, his bundle; LAF, left anterior fascicle; LPF, left pos-
terior fascicle; RB, right bundle. (From Nogami A.
Purkinje-related arrhythmias part I: monomorphic
ventricular tachycardias. Pacing Clin Electrophysiol
2011;34:643; with permission.)
Fig. 10. Patient with frequent and multifocal premature ventricular contractions (PVCs) emanating from
throughout the conduction system. Note the narrow QRS morphologies of the PVCs and varying axes.
may be remote from the VT exit site into the ven-
tricular myocardium.25 Pacing at successful abla-
tion sites often captures both local myocardial
tissue and the Purkinje fiber system, generating a
QRS morphology that can be very different from
the QRS morphology of the clinical VT, whereas
pacing at a distal location closer to the myocardial
breakthrough site may provide an excellent match
with the targeted VT but may not represent an
effective ablation site (Fig. 14). Some investiga-
tors, however, have described ablation of the
more distally located Purkinje-myocardial inter-
face. Effective ablations have been described us-
ing this area as a target; however, more
extensive ablation lesions are required here to
render VT noninducible, most likely because of
arborization of the distal Purkinje fiber system.26
An advantage of this technique is that the conduc-
tion in the fascicular system is not impaired
postablation.
Another ablation strategy during sinus rhythm
targets the area of slow conduction that is adja-
cent to the posterior fascicle. At these sites, both
low-amplitude electrograms attributable to the
slow conduction zone and sharp and more prom-
inent Purkinje potentials are present (see
Fig. 11).22 Conduction through the distal portion
of the slow conduction zone during sinus rhythm
is believed retrograde and the identification of
the earliest of these retrograde signals has been
 Fascicular Tachycardia 575

Fig. 11. Identification of the left posterior fascicle and slow conduction zone during sinus rhythm in patients with
idiopathic fascicular tachycardia. Note that the slow conduction zone characterized with diastolic potentials (DPs)
is located within the inferoposterior septum and marked with green tags; the area with Purkinje potentials (PP) is
located within the posterior septum and marked with pink tags. The black line delineates part of the left poste-
rior fascicle and the red line represents the slow conduction zone. From the intracardiac electrograms ad, the
arrows indicate the PP, the asterisks indicate the DP. (A) Right anterior oblique view. (B) Left anterior oblique
view. (C) Mesh mapping at right anterior oblique view. (D) The electroanatomic map of the effective target
site. (From Chu J, Sun Y, Zhao Y, et al. Identification of the slow conduction zone in a macroreentry circuit of
verapamil-sensitive idiopathic left ventricular tachycardia using electroanatomic mapping. J Cardiovasc Electro-
physiol 2012;23:841; with permission.)

proposed as the ideal ablation target when
ablating during sinus rhythm.21 In many patients,
however, the lower-amplitude signals associated
with a proposed slow conduction zone are either
not identified or similar nonspecific electrograms
are seen ubiquitously throughout the ventricular
chamber.
Yet another ablation strategy, particularly useful
in patients in whom sustained VT is not inducible,
is the empiric creation of a linear lesion set perpen-
dicular to the long axis of the ventricle at the mid-
to midinferior septum. Ablation here is likely to
transect the reentrant circuit and has been shown
to have favorable outcomes, albeit with risk of left
posterior fascicular block.27 The long-term ramifi-
cations of such a block are not clear and creating
a block has been proposed as an effective
endpoint to ablation.
Targeted endpoints to the ablation can vary and
can include termination of induced tachycardia,
noninducibility, ablation, and possible elimination
of target electrograms during sinus rhythm, or
development of left posterior fascicular block.
Wissner and colleagues28 targeted ablation at
the earliest retrograde Purkinje potential primarily
during sinus rhythm in 24 patients and showed a
92% arrhythmia-free survival at a median of
8.9 years follow-up with no patients suffering a
left posterior fascicular block. In a recent study
by Kataria and colleagues,26 the distal posterior
fascicle was targeted until block was achieved
from the local myocardium to the fascicle and
100% arrhythmia-free survival was reported in 15
patients at a mean follow-up of 20.8 months. Over-
all, long-term success rates seem generally high
and exceed 90% to 95%.29 Although complication
rates are difficult to accurately ascertain due to the
limited sample sizes, most studies report no or
rare complications.29 In particular, atrioventricular
block is very rare due to the distal ablation targets
and left posterior fascicular block may or may not
be an intended goal of ablation.
576 Latchamsetty & Bogun

Fig. 12. Schematic illustration of the reentrant circuit of idiopathic fascicular tachycardia. During tachycardia, conduc-
tion is antegrade through a zone of slow conduction and retrograde over the left posterior fascicle (LPF). Low-
amplitude signals (DP) at the terminal end of the slowly conducting limb or sharp and early Purkinje potentials (PP)
are potential ablation targets during tachycardia. (Adapted from Aiba T, Suyama K, Aihara N, et al. The role of Purkinje
and pre-Purkinje potentials in the reentrant circuit of verapamil-sensitive idiopathic LV tachycardia. Pacing Clin Electro-
physiol 2001;24:342; with permission.)

Despite involvement of similar anatomic struc- from the fascicles or the Purkinje fiber system,
tures, ablation strategies and targets for other ven- mapping of the earliest Purkinje potential during
tricular arrhythmias from the Purkinje system can PVCs identifies the site of origin where radiofre-
be quite different. In patients with PVCs originating quency energy can be applied (Fig. 15). In patients

Fig. 13. Successful site of ablation terminating fascicular tachycardia. Note the presence of both a sharp Purkinje
potential (PP) as well as a late and low-amplitude diastolic potential (DP) on the ablation electrogram.
 Fascicular Tachycardia 577

Fig. 14. (A) Pacemapping performed on a patient with fascicular tachycardia involving the anterior fascicle re-
vealed an excellent match to the clinical ventricular tachycardia (VT) at the site of exit to the ventricular myocar-
dium. Ablation here had no effect on the VT. Note the local electrogram recorded from the distal ablation
catheter preceded the QRS complex by 20 ms. (B) Pace mapping from the site of the earliest sharp Purkinje po-
tentials during tachycardia revealed a poor match to the clinical VT due to capture of local myocardial tissue in
addition to the anterior fascicle. The local Purkinje potential during VT on the distal ablation catheter (arrow)
preceded the QRS complex by 30 ms and ablation here resulted in termination of the VT. (From Bogun F,
El-Atassi R, Daoud E, et al. Radiofrequency ablation of idiopathic left anterior fascicular tachycardia. J Cardiovasc
Electrophysiol 1995;6:1114, 1115; with permission.)

with prior myocardial infarction and VT with an exit containing fascicular potentials can be targeted
site involving the fascicular system, parts of the (see Fig. 8). The presence of concealed entrain-
reentrant circuit (often located within the inferior ment with matching stimulus-QRS and
wall scar when the posterior fascicle is involved electrogram-QRS intervals helps to identify critical
in the VT exit) can be targeted or the exit site components of the reentry circuit.11
578 Latchamsetty & Bogun

Fig. 15. Activation map in a patient with frequent premature ventricular contractions (PVCs) identified the site of
origin in the left posterior fascicle. At this successful ablation site, during PVCs a sharp and early Purkinje poten-
tial (arrow) is seen on the distal ablation catheter (Map d) electrogram. HRA, high right atrium; Map p, proximal
ablation.

SUMMARY who prefer to avoid long-term pharmacologic ther-

Fascicular VT is a reentrant tachycardia involving
most commonly the left posterior fascicle with an
overall favorable prognosis. Patients most
commonly present with palpitations during exer-
cise although the arrhythmia can also present at
rest. Rarely, fascicular tachycardia is incessant
and causes a tachycardia-mediated cardiomyop-
athy. Sudden cardiac death is not typically seen
with this arrhythmia. Diagnosis is suggested by
characteristic findings on ECG and confirmed
through electrophysiology study. The rhythm is
acutely susceptible to medical management
most commonly with intravenous verapamil.
Long-term management can be attempted with
oral calcium channel blockade with varying ac-
counts of success. Catheter ablation has a high
curative rate with infrequent complications and
can be considered in patients refractory to medical
management or as a first-line therapy in patients
apy or in whom medical management my be con-
traindicated. Ablation targets and endpoints are
varied but suitable targets can be identified during
tachycardia or sinus rhythm.
REFERENCES
1. Cohen HC, Gozo EG, Pick A. Ventricular tachycardia
with narrow QRS complexes (left posterior fascicular
tachycardia). Circulation 1972;45:103543.
2. Morgera T, Hrovatin E, Mazzone C, et al. Clinical
spectrum of fascicular tachycardia. J Cardiovasc
Med (Hagerstown) 2013;14:7918.
3. Zipes D, Jalife J, Lerman B. Cardiac electrophysi-
ology, from cell to bedside. Philadelphia: Saunders
Elsevier; 2009.
4. Velazquez-Rodrguez E, Rodrguez-Pina H, Pa-
checo-Bouthillier A, et al. Cardiomyopathy induced
by incessant fascicular ventricular tachycardia.
Arch Cardiol Mex 2013;83:1948.

5. Nogami A. Purkinje-related arrhythmias part I:
monomorphic ventricular tachycardias. Pacing Clin
Electrophysiol 2011;34:62450.
6. Nogami A. Idiopathic left ventricular tachycardia:
assessment and treatment. Card Electrophysiol
Rev 2002;6:44857.
7. Good E, Desjardins B, Jongnarangsin K, et al. Ven-
tricular arrhythmias originating from a papillary mus-
cle in patients without prior infarction: a comparison
with fascicular arrhythmias. Heart Rhythm 2008;5:
15307.
8. Yokokawa M, Good E, Desjardins B, et al. Predictors
of successful catheter ablation of ventricular arrhyth-
mias arising from the papillary muscles. Heart
Rhythm 2010;7(11):16549.
9. Thakur RK, Klein GJ, Sivaram CA, et al. Anatomic
substrate for idiopathic left ventricular tachycardia.
Circulation 1996;93:497501.
10. Suwa M, Yoneda Y, Nagao H, et al. Surgical correc-
tion of idiopathic paroxysmal ventricular tachycardia
possibly related to left ventricular false tendon. Am J
Cardiol 1989;64:121720.
11. Bogun F, Good E, Reich S, et al. Role of purkinje fi-
bers in post-infarction ventricular tachycardia. J Am
Coll Cardiol 2006;48:25007.
12. Josephson M. Clinical cardiac electrophysiology,
techniques and interpretations. Philadelphia: Lippin-
cott Williams & Wilkins; 2008.
13. Hassaguerre M, Shoda M, Jas P, et al. Mapping
and ablation of idiopathic ventricular fibrillation. Cir-
culation 2002;106:9627.
14. Laurent G, Saal S, Amarouch MY, et al. Multifocal
ectopic purkinje-related premature contractions: a
new scn5a-related cardiac channelopathy. J Am
Coll Cardiol 2012;60:14456.
15. Tsuchiya T, Okumura K, Honda T, et al. Effects of
verapamil and lidocaine on two components of the
re-entry circuit of verapamil-senstitive idiopathic
left ventricular tachycardia. J Am Coll Cardiol
2001;37:141521.
16. Griffith MJ, Garratt CJ, Rowland E, et al. Effects of
intravenous adenosine on verapamil-sensitive idio-
pathic ventricular tachycardia. Am J Cardiol 1994;
73:75964.
17. Chiaranda` G, Di Guardo G, Gulizia M, et al. Fascic-
ular ventricular tachycardia. Ital Heart J Suppl 2001;
2:11816 [in Italian].
18. Ruffy R, Kim SS, Lal R. Paroxysmal fascicular tachy-
cardia: electrophysiologic characteristics and treat-
ment by catheter ablation. J Am Coll Cardiol 1985;
5:100814.
Fascicular Tachycardia 579
19. Belhassen B, Rotmensch HH, Laniado S. Response
of recurrent sustained ventricular tachycardia to
verapamil. Br Heart J 1981;46:67982.
20. Kottkamp H, Chen X, Hindricks G, et al. Radiofre-
quency catheter ablation of idiopathic left ventricular
tachycardia: further evidence for microeentry as the
underlying mechanism. J Cardiovasc Electrophysiol
1994;5:26873.
21. Ouyang F, Cappato R, Ernst S, et al. Electroanatomic
substrate of idiopathic left ventricular tachycardia:
unidirectional block and macroreentry within the pur-
kinje network. Circulation 2002;105:4629.
22. Chu J, Sun Y, Zhao Y, et al. Identification of the slow
conduction zone in a macroreentry circuit of
verapamil-sensitive idiopathic left ventricular tachy-
cardia using electroanatomic mapping. J Cardiovasc
Electrophysiol 2012;23:8405.
23. Aiba T, Suyama K, Aihara N, et al. The role of pur-
kinje and pre-purkinje potentials in the reentrant cir-
cuit of verapamil-sensitive idiopathic LV tachycardia.
Pacing Clin Electrophysiol 2001;24:33344.
24. Schreiber D, Kottkamp H. Ablation of idiopathic
ventricular tachycardia. Curr Cardiol Rep 2010;12:
3828.
25. Bogun F, El-Atassi R, Daoud E, et al. Radiofrequency
ablation of idiopathic left anterior fascicular tachy-
cardia. J Cardiovasc Electrophysiol 1995;6:11136.
26. Kataria V, Yaduvanshi A, Kumar M, et al. Demonstra-
tion of posterior fascicle to myocardial conduction
block during ablation of idiopathic left ventricular
tachycardia: an electrophysiological predictor of
long-term success. Heart Rhythm 2013;10:63845.
27. Lin D, Hsia HH, Gerstenfeld EP, et al. Idiopathic
fascicular left ventricular tachycardia: linear ablation
lesion strategy for noninducible or nonsustained
tachycardia. Heart Rhythm 2005;2:9349.
28. Wissner E, Menon SY, Metzner A, et al. Long-term
outcome after catheter ablation for left posterior
fascicular ventricular tachycardia without develop-
ment of left posterior fascicular block. J Cardiovasc
Electrophysiol 2012;23:117984.
29. Aliot EM, Stevenson WG, Almendral-Garrote JM,
et al. EHRA/HRS expert consensus on catheter
ablation of ventricular arrhythmias: developed in a
partnership with the European Heart Rhythm Associ-
ation (EHRA), a Registered Branch of the European
Society of Cardiology (ESC), and the Heart Rhythm
Society (HRS); in collaboration with the American
College of Cardiology (ACC) and the American
Heart Association (AHA). Heart Rhythm 2009;6:
886933.